Henry Ginard, Li Wei, Garner Warren, Woodley David T
Division of Plastic Surgery, Department of Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Lancet. 2003 Feb 15;361(9357):574-6. doi: 10.1016/S0140-6736(03)12510-X.
When skin is wounded, human keratinocytes at the wound edge stop differentiating and start migrating to resurface the wound. How this change takes place is unclear. Because keratinocytes at the wound edge are for the first time surrounded by serum rather than plasma, serum could contain some migration-promoting factor or factors that is absent in plasma. We did standard computer-assisted in-vitro migration assays of human keratinocytes in the presence of either human plasma or serum. We also did a semiquantitative western blot analysis to determine if p38 mitogen-activated protein kinase (p38MAPK) was activated by either serum or plasma. Our results showed that keratinocytes migrating on collagen in the presence of serum produced migration indices in the range of 28, whereas those in the presence of plasma were about 12--the same level as control assays without either serum or plasma. We also showed that induced keratinocyte polarisation, activation of p38MAPK, and production of matrix metalloprotease 9 are possible mechanisms for promotion of re-epithelialisation of skin wounds by human serum.
皮肤受伤时,伤口边缘的人类角质形成细胞会停止分化并开始迁移,以重新覆盖伤口表面。这种变化是如何发生的尚不清楚。由于伤口边缘的角质形成细胞首次被血清而非血浆包围,血清可能含有一些血浆中不存在的促进迁移的因子。我们在存在人血浆或血清的情况下,对人角质形成细胞进行了标准的计算机辅助体外迁移试验。我们还进行了半定量蛋白质印迹分析,以确定血清或血浆是否激活了p38丝裂原活化蛋白激酶(p38MAPK)。我们的结果表明,在血清存在下在胶原蛋白上迁移的角质形成细胞产生的迁移指数在28左右,而在血浆存在下的迁移指数约为12,与没有血清或血浆的对照试验水平相同。我们还表明,诱导角质形成细胞极化、激活p38MAPK以及产生基质金属蛋白酶9可能是人类血清促进皮肤伤口重新上皮化的机制。